Search

Background and Objective The course of atrial septal defects (ASD) in children undergoing liver transplantation is poorly described. Our objective was to present our experience in living donor liver transplantation (LDLT) in children with type II ASD. Patients and Methods Between June 1994 and December 2006, 18/140 (12.8%) pediatric LDLT were diagnosed to have both type II ASD and end-stage liver disease. We reviewed the records of these patients. The median follow-up was 48.7 months. Data were analyzed using descriptive statistics. Results There were 8 male and 10 female patients whose overall mean age was 12 months. There were 15 biliary atresia and 3 neonatal hepatitis patients. The median Child score was 9. The mean Pediatric Model End-stage Liver Disease score was 14. There were 13 with small (≤4 mm), 4 with medium (5 to 9 mm), and 1 large (>10 mm) ASD. Six small ASD closed spontaneously pretransplant. Seven small ASD closed posttransplant. The medium and large ASD persisted or increased in size posttransplant. Only one patient showed hemodynamically significant ASD based on cardiac echocardiography and catheterization. This patient underwent Amplatzer closure of the ASD at 10 months posttransplant. All patients are surviving with their original grafts to date. There were no perioperative cardiac or neurologic complications. Conclusion This series demonstrated that LDLT can be safely performed in hemodynamically stable patients with small- to large-sized ASD. Small ASD may close pre- or posttransplant.

Administration of donor-derived immature dendritic cells (DC) treated with transforming growth factor-beta (TGF-beta) to prevent allograft rejection is not applicable for clinical use. We therefore attempted to explore the use of recipient-derived DC pulsed with donor antigens via the indirect pathway (cross-priming). DC were propagated from C3H (H2(k)) bone marrow (BM) using granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-4 (IL-4). TGF-beta (0.2 ng/mL) was added at the initiation of culture. The resultant TGF-beta DC were pulsed with B10 (H2(b)) splenocyte lysate. Expression of major histocompatibility complex (MHC) class I and II was not affected, while CD40, CD80, and CD86 costimulatory molecules on DC were significantly inhibited by treatment with TGF-beta. C3H DC pulsed with B10 antigens stimulated a proliferative response in C3H T cells which was inhibited when DC were treated with TGF-beta, and the cytotoxic T-lymphocyte (CTL) activity was also inhibited. This observation correlated with reduced interferon-gamma (IFN-gamma) and increased IL-10 production. A single injection of TGF-beta DC prolonged allograft survival (median survival time [MST] 18 days vs 10 days in no-DC treatment control; P.05). These data indicated that an approach utilizing recipient DC as a "vaccine" strategy is possible.